{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhou Y"],"funding":["Natural Science Foundation of Zhejiang Province","Youth Cultivation Plan 'Cultivation Star Project' of Shanghai Jiao Tong University School of Medicine Affiliated Ruijin Hospital","National Natural Science Foundation of China","Zhejiang Provincial Science and Technology Innovation Program","Zhejiang Provincial Science and Technology Innovation Program (New Young Talent Program) for College Students","Characteristic Directional S-Disciplines of The First Affiliated Hospital of Wenzhou Medical University","Science and Technology Project of Wenzhou","Health Commission of Zhejiang Province"],"pagination":["e70621"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12940804"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(3)"],"pubmed_abstract":["<h4>Background</h4>Ageing is a significant risk factor for pathophysiological alterations in the heart, but the intrinsic mechanisms by which these occur have yet to be fully elucidated. Purinergic 2×7 receptor (P2X7R) is important for the pathogenesis of numerous cardiovascular diseases; nevertheless, its function in the process of cardiac ageing remains uncertain.<h4>Methods</h4>This study utilised P2X7R knockout (P2X7R<sup>-</sup>/<sup>-</sup>) mice. An ageing model was established by either maintaining mice until they reached 20 months of age or performing chronic subcutaneous injection of D-galactose (D-gal). Recombinant adeno-associated virus serotype 9 (AAV9) was employed to achieve cardiac-specific overexpression of P2X7R and nuclear receptor subfamily 4 group A member 1 (NR4A1). C"],"journal":["Clinical and translational medicine"],"pubmed_title":["P2X7R deficiency alleviates cardiac senescence by enhancing mitophagy via the HuR/TRIM26/NR4A1 axis."],"pmcid":["PMC12940804"],"funding_grant_id":["2024R413C089","80225018","ZCLMS26H0201","wyyy-2025S02","82570459","Y20240070","82202380","WKJ-ZJ-2540","2024PY192","Y2023127"],"pubmed_authors":["Shen J","Zhang J","Ye B","Zhong X","Zhou Y","Zhang W","Xing J","Yang Z","Huang Z","Mei J","Chen Y","Lin J","Wang Y","Wang Z","Mao Z"],"additional_accession":[]},"is_claimable":false,"name":"P2X7R deficiency alleviates cardiac senescence by enhancing mitophagy via the HuR/TRIM26/NR4A1 axis.","description":"<h4>Background</h4>Ageing is a significant risk factor for pathophysiological alterations in the heart, but the intrinsic mechanisms by which these occur have yet to be fully elucidated. Purinergic 2×7 receptor (P2X7R) is important for the pathogenesis of numerous cardiovascular diseases; nevertheless, its function in the process of cardiac ageing remains uncertain.<h4>Methods</h4>This study utilised P2X7R knockout (P2X7R<sup>-</sup>/<sup>-</sup>) mice. An ageing model was established by either maintaining mice until they reached 20 months of age or performing chronic subcutaneous injection of D-galactose (D-gal). Recombinant adeno-associated virus serotype 9 (AAV9) was employed to achieve cardiac-specific overexpression of P2X7R and nuclear receptor subfamily 4 group A member 1 (NR4A1). C","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Mar","modification":"2026-07-16T21:55:48.395Z","creation":"2026-07-10T03:16:26.906Z"},"accession":"S-EPMC12940804","cross_references":{"pubmed":["41746668"],"doi":["10.1002/ctm2.70621"]}}